Systems Pharmacology-based Analysis of Anti-tumor Mechanism of Houttuynia cordata
10.13422/j.cnki.syfjx.20220819
- VernacularTitle:基于系统药理学分析鱼腥草抗肿瘤作用机制
- Author:
Yuru ZHANG
1
;
Xuping TIAN
1
;
Zezhou ZHAO
1
;
Wei XIAO
2
;
Yonghua WANG
1
Author Information
1. Shihezi University，Shihezi 832000，China
2. Jiangsu Kanion Pharmaceutical Co. Ltd.，Lianyungang 222000，China
- Publication Type:Journal Article
- Keywords:
Houttuynia cordata;
lung cancer;
systems pharmacology;
cell cycle
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2022;28(14):165-171
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo explore the effective components， targets， and mechanism of Houttuynia cordata against lung cancer by means of systems pharmacology and further to provide a reference for the further development and clinical application of this medicinal. MethodChemical components of H. cordata were retrieved from Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP） and the active components were screened based on oral bioavailability （OB） and drug-likeness （DL）. Then the potential targets were predicted， followed by enrichment analysis. Finally， sodium houttuyfonate （SH） was selected for verifying the anti-tumor mechanism. Cell counting kit-8 （CCK-8） assay was used to evaluate the effect of SH on the in vitro proliferation of two lung cancer cell lines： A549 and LLC， and the regulation of tumor-related proteins by SH was verified by Western blot. ResultA total of 7 active compounds and 352 targets of the active components were screened out. According to the enrichment analysis of targets， H. cordata had potential therapeutic effects on cancer. SH had inhibitory effect on both A549 and LLC. Western blot results showed that G1/S-specific Cyclin D1， E1 and cyclin-dependent kinase （CDK）2， CDK4 all tended to be down-regulated， and Janus kinase 2 （JAK2）/signal transducer and activator of transcription 3 （STAT3） also changed significantly. ConclusionH. cordata has the potential anti-tumor effects by arresting the tumor cells in the G1 phase through the JAK2/STAT3 pathway.
